Introduction

Uses for Prednisolone Sodium Phosphate

Treatment of a wide variety of diseases and conditions, principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases.c

Adrenocortical Insufficiency

Corticosteroids are administered in physiologic dosages to replace deficient endogenous hormones in patients with adrenocortical insufficiency.c

Because production of both mineralocorticoids and glucocorticoids is deficient in adrenocortical insufficiency, hydrocortisone or cortisone (in conjunction with liberal salt intake) usually is the corticosteroid of choice for replacement therapy.ac

Usually inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.bc

If prednisolone is used for adrenocortical insufficiency, a mineralocorticoid (e.g., fludrocortisone) must also be administered, particularly in infants.abcdg

Adrenogenital Syndrome

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; concomitant use of a mineralocorticoid may be necessary until the patient is at least 5–7 years of age.c

For long-term therapy after early childhood, a glucocorticoid alone usually is sufficient.c

May be used as maintenance therapy (e.g., in rheumatoid arthritis, acute gouty arthritis, systemic lupus erythematosus, acute rheumatic carditis) as part of a total treatment program in selected patients when more conservative therapies have proven ineffective.acdg

Glucocorticoid withdrawal is extremely difficult if used for maintenance; relapse and recurrence usually occur with drug discontinuance.c

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.c

Adjunctively for severe systemic complications of Wegener’s granulomatosis†, but cytotoxic therapy is the treatment of choice.c

Primary treatment to control symptoms and prevent severe, often life-threatening complications of systemic lupus erythematosus, systemic dermatomyositis (polymyositis), polyarteritis nodosa†, relapsing polychondritis, polymyalgia rheumatica, Sjogren's syndrome, giant-cell (temporal) arteritis†, certain cases of vasculitis, or mixed connective tissue disease syndrome†.acde High dosage may be required for acute situations; after a response has been obtained, the drug must often be continued for long periods at low dosage.c

Polymyositis† associated with malignancy and childhood dermatomyositis may not respond well.c

Allergic Conditions

For control of severe or incapacitating allergic conditions unresponsive to adequate trials of conventional treatment; for control of acute manifestations, including angioedema†, serum sickness, allergic symptoms of trichinosis†, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.acdg

Systemic therapy usually reserved for acute conditions and severe exacerbations.c

For acute conditions, usually used in high dosage and with other therapies (e.g., antihistamines, sympathomimetics).c

Reserve prolonged treatment of chronic allergic conditions to disabling conditions unresponsive to more conservative therapy and when risks of long-term glucocorticoid therapy are justified.c

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.c

Acute optic neuritis optimally treated with initial high-dose IV (e.g., methylprednisolone) therapy followed by chronic oral corticosteroid therapy. Aids in recovery of vision and slows progression to clinically definite multiple sclerosis. In a randomized, placebo-controlled trial, oral corticosteroid (e.g., prednisone) monotherapy did not improve the rate of vision recovery and was associated with an increased risk of new episodes of optic neuritis in either eye.

Less severe allergic and inflammatory allergic conditions of the eye are treated with topical ophthalmic corticosteroids.f

Systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.c

Asthma

Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.cde

Corticosteroids used systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.j

Because onset of effects is delayed, do not use alone for emergency treatment.c

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.f

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.c

In hospital management of an acute asthma exacerbation, use systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.c

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthmac (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).b

Chronic Obstructive Pulmonary Disease

For severe exacerbations of chronic obstructive pulmonary disease (COPD),d a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.e

Much less dramatic effects in stable COPD than in asthma, and the role of glucocorticoids is limited to very specific indications.p

In acute tuberculous pericarditis, systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion).

In tuberculous pleurisy, hastens the resolution of pain, dyspnea, and fever.

Used adjunctively with antimycobacterial agents for the treatment of tuberculosis with enlarged mediastinal lymph nodes causing respiratory difficulty.d The safety and efficacy of adjunctive glucocorticoid therapy in patients with tuberculous lymphadenitis, miliary or laryngeal tuberculosis, or HIV-associated tuberculosis has not been fully elucidated.

Hypersensitivity Pneumonitis

Pulmonary Fibrosis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids.c

>Pneumocystis carinii Pneumonia

Used adjunctively with appropriate anti-infective therapy in the management of moderate to severe Pneumocystis carinii pneumonia in patients with acquired immunodeficiency syndrome (AIDS) to decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death.

Berylliosis

Aspiration Pneumonitis

Anthrax

Adjunct to anti-infective therapy in the treatment of anthrax† in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

Used for cutaneous anthrax† if there are signs of systemic involvement or extensive edema involving the neck and thoracic region. Has been used for anthrax meningitis†, and inhalational anthrax† that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis or regional enteritis, or celiac disease†.acdg Low dosages of glucocorticoids, in conjunction with other supportive therapy, may occasionally be useful for patients unresponsive to usual therapy for chronic conditions.c

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.d

Crohn’s Disease

Management of mildly to moderately active and moderately to severely active Crohn’s disease.a

Some experts state that conventional glucocorticoids should not be used for the management of mildly to moderately active disease because of their high incidence of adverse effects, and their use should be reserved for patients with moderately to severely active disease.

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease†. Once patients respond to parenteral therapy, they should gradually be switched to an equivalent regimen of an oral glucocorticoid.

Glucocorticoids should not be used for maintenance therapy of Crohn’s disease because they usually do not prevent relapses and the drugs may produce severe adverse reactions with long-term administration.

Glucocorticoids have been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease† in pediatric patients.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).adef

In adults, acute lymphocytic (lymphoblastic) leukemia, chronic lymphocytic leukemia, and Hodgkin’s disease respond well to combination regimens that include a glucocorticoid (usually prednisone or prednisolone).c Acute myeloblastic leukemia, lymphosarcoma, and the blast crisis of chronic myelocytic leukemia may fail to respond or may relapse upon discontinuance of therapy.c

Treatment of breast cancer†:e Glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.c

Glucocorticoids alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer†.e

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria† caused by Plasmodium falciparum; no longer recommended for this condition.cd

Liver Disease

In patients with subacute hepatic necrosis† and chronic active hepatitis†,e high-dose glucocorticoids can decrease serum bilirubin, ascites, and mortality rate.c In nonalcoholic cirrhosis† in women,e the drugs increase survival rate in the absence of ascites, but not when ascites is present.c May decrease mortality rate in patients with alcoholic cirrhosis with hepatic encephalopathy†, but should not be used in less seriously ill patients.c

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis.ad Have replaced corticotropin as the therapy of choice because of a more rapid onset of action, more consistent effects, and fewer adverse effects.

Prednisolone Sodium Phosphate Dosage and Administration

General

Route of administration and dosage depend on the condition being treated and the patient response.a

Alternate-day Therapy

Alternate-day therapy in which a single dose (twice the usual daily dosage) is administered every other morning is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions.ac This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.ac

If alternate-day therapy is preferred, only use a “short-acting” glucocorticoid that suppresses the HPA axis <1.5 days after a single oral dose (e.g., prednisone, prednisolone, methylprednisolone).c

Discontinuance of Therapy

A steroid withdrawal syndrome consisting of lethargy, fever, myalgia can develop following abrupt discontinuance.c Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly).c

If used for only brief periods (a few days) in emergency situations, may reduce and discontinue dosage quite rapidly.cg

In 1 suggested regimen, decrease by 2.5–5 mg every 3–7 days until the physiologic dose (5 mg) is reached.c

Other recommendations state that decrements usually should not exceed 2.5 mg every 1–2 weeks.c

When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient has been receiving.c After 2–4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily is reached.c

For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days).c Administer a high dose on the first day of therapy, then withdraw therapy by tapering the dosage over several days.c

Administration

Oral Administration

Dosage

Dosage of prednisolone sodium phosphate is expressed in terms of prednisolone.abd

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.b

Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma).b

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases.c After a response has been obtained, drug often must be continued for long periods at low dosage.c

High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides.c Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris.c Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible.c

Pediatric Patients

Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area.b

Usual Dosage

Oral

Asthma

Oral

For the treatment of refractory bronchial asthma and related bronchospasm (severe persistent asthma) not controlled with high maintenance dosages of an inhaled corticosteroid and a long-acting bronchodilator, add an oral corticosteroid (e.g., prednisone, prednisolone, methylprednisolone) at a dosage of 1–2 mg/kg daily in single or divided doses.d Continue a short course of oral corticosteroid therapy (usually 3–10 days) until a peak expiratory flow rate of 80% of personal best is achieved or until symptoms resolve.d May need a longer duration of treatment in some children.d No evidence that tapering the dosage after improvement will prevent relapse.d

Nephrotic Syndrome

Oral

Usual dosage: 60 mg/m2 given in 3 divided doses for 4 weeks, followed by 4 weeks of alternate-day therapy at single doses of 40 mg/m2.d

Adults

Usual Dosage

Oral

Initially, 5–60 mg daily, depending on the disease being treated; usually administered in 2–4 divided doses.bdg

Acute Exacerbations of Multiple Sclerosis

Oral

Usual dosage: 200 mg daily for 1 week, followed by 80 mg every other day for a month.bd

Cautions for Prednisolone Sodium Phosphate

Contraindications

Known hypersensitivity to prednisolone, any ingredient in the respective formulation, or any other corticosteroid.cd

Concurrent administration of live or live, attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids.d (See Specific Drugs under Interactions.)

Warnings/Precautions

Warnings

Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).c

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.c

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.c

Withdraw prednisolone very gradually following long-term therapy with pharmacologic dosages.c (See Discontinuance of Therapy under Dosage and Administration: Dosage.)

Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods.c

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma, illness) and replacement therapy may be required.acdg Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid also should be administered.cd

If the disease flares up during withdrawal, may need to increase dosage temporarily and then withdraw drug more gradually.c

Immunosuppression

Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression.d Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients.d (See Increased Susceptibility to Infection under Warnings.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.do In addition, if inactivated viral or bacterial vaccines are administered to such patients, expected serum antibody response may not be obtained.acd The USPHS Advisory Committee on Immunization Practices (ACIP) and American Academy of Family Physicians (AAFP)o state that administration of live virus vaccines usually is not contraindicated in patients receiving corticosteroid therapy under the following circumstances:

short-term (<2 weeks) therapy

low to moderate dosage

long-term alternate-day treatment with long-acting preparations

maintenance physiologic dosages (replacement therapy)

if it is administered topically, ophthalmically, intra-articularly, bursally, or into a tendono

Increased Susceptibility to Infection

Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection.d

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system may be associated with glucocorticoids alone or in combination with other immunosuppressive agents.

Infections may be mild, but they can be severe or fatal, and localized infections may disseminate.

Do not use, except in life-threatening situations, in patients with viral infections, or bacterial infections not controlled by anti-infectives.c

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.d

Children and adults who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.d

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba).d

Use with great care in patients with known or suspected Strongyloides (threadworm) infection.d Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

Not effective and can have detrimental effects in the management of cerebral malaria.cd

Can reactivate tuberculosis.d Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy.cd Observe closely for evidence of reactivation.d Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate antimycobacterial chemotherapy.d

Can reactivate latent amebiasis.cd Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.cd

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids.cd These adverse effects may be especially serious in geriatric or debilitated patients.c A high protein diet may help to prevent adverse effects associated with protein catabolism.c

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium).add

Tendon rupture, particularly of the Achilles tendon.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) currently considers patients receiving or planning to receive the equivalent of at least 5 mg of prednisone (i.e., 5 mg of prednisolone) daily for 3 months or longer to be at risk for bone loss.

To minimize the risk of glucocorticoid-induced bone loss, should use the smallest possible effective dosage and duration and use topical and inhaled preparations whenever possible. Obtain baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and initiate appropriate preventive therapy. May repeat longitudinal measurements as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

Before initiating glucocorticoid therapy in postmenopausal women, consider that they are especially prone to osteoporosis.cd

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.c

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur but is less common with prednisolone than with average or large doses of cortisone or hydrocortisone.d Risk is increased with high-dose synthetic glucocorticoids for prolonged periods.cd Edema and CHF (in susceptible patients) may occur.c

Dietary salt restriction is advisable and potassium supplementation may be necessary.cd

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve.d If corticosteroid therapy is continued for >6 weeks, monitor IOP.d

May enhance the establishment of secondary fungal, bacterial, and viral infections of the eye.d

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.cd

Endocrine and Metabolic Effects

With prolonged therapy, may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.acd

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus.acg If glucocorticoid therapy is required in patients with diabetes mellitus, may be necessary to change insulin or oral antidiabetic agent dosage or diet.acg

GI Effects

Use with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses.d

Signs of peritoneal irritation following GI perforation may be absent in patients receiving corticosteroids.cd

Use with caution in patients with active or latent peptic ulcer.d Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids.c

Dermatologic Effects

Kaposi’s sarcoma has been reported to occur in patients receiving glucocorticoid therapy; discontinuance of such therapy may result in remission of the disease.d

Specific Populations

Pregnancy

Category C.d If substantial dosage is received during pregnancy, carefully observe infant for signs of hypoadrenalism.d

Lactation

Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants.cd Use with caution.d

Pediatric Use

The effects of glucocorticoids on the pathophysiology and course of diseases are considered to be similar in adults and children.cd Evidence of safety and efficacy for prednisolone in pediatric patients based on treatment of nephrotic syndrome (in patients older than 2 years of age) and aggressive leukemias and lymphomas (in patients older than 1 month of age).cd Evidence of safety and efficacy for other pediatric indications (e.g., severe asthma and wheezing) are based on controlled trials in adults.cd

The adverse effects in pediatric patients are similar to those in adults.c As in adults, perform periodic evaluations of height, weight, ocular pressure, and BP.cd Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.cd

With long-term use, may delay growth and maturation in children and adolescents.cd Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.acd Titrate dosage to the lowest effective level.cd Alternate-day therapy with glucocorticoids that cause shorter HPA-axis suppression than does dexamethasone (e.g., prednisone, prednisolone, methylprednisolone) may minimize growth suppression and should be instituted if growth suppression occurs.c

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DEXA]) in children and adolescents are similar to those in adults.

Ensure children and adolescents consistently ingest adequate calcium and vitamin D, either through diet or supplementation.

Geriatric Use

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur.c May be especially serious in geriatric or debilitated patients.c

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.c

With indomethacin and prednisolone administration, plasma concentrations of free prednisolone were increased; total plasma prednisolone concentrations were unchanged.c Indomethacin may have a steroid-sparing effectc

May need to decrease dosage of concomitant corticosteroids to avoid potential adverse effectsc

Vaccines and toxoids

May cause a diminished response to toxoids and live or inactivated vaccinescd

May potentiate replication of some organisms contained in live, attenuated vaccinesc

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages) c

(See Immunosuppression under Cautions)

Prednisolone Sodium Phosphate Pharmacokinetics

Absorption

Onset

Following oral administration in patients with asthma, effects may not be evident for several hours.

Duration

The duration of anti-inflammatory activity of prednisolone approximately equals the duration of HPA-axis suppression, about 1.25–1.5 days for a single 50-mg oral dose.c

Distribution

Extent

Most corticosteroids removed rapidly from blood and distributed to muscles, liver, skin, intestines, and kidneys.c Distribute into breast milk and placenta.c

Plasma Protein Binding

Has a high affinity for transcortin and competes with cortisol for binding to this binding protein.c Because only unbound drug is pharmacologically active, patients with low serum albumin concentrations may be more susceptible to glucocorticoid effects.c

Elimination

Metabolism

Corticosteroids metabolized in most tissues, but primarily in liver, to inactive compounds.c

Special Populations

In patients with hypothyroidism, metabolic clearance of corticosteroids decreased.d

In patients with hyperthyroidism, metabolic clearance of corticosteroids increased.d

Changes in thyroid status may necessitate adjustment of glucocorticoid dosage.d

Advice to Patients

In patients receiving long-term therapy, importance of not discontinuing the drug abruptly.d

Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.c

Importance of carrying identification cards listing the diseases being treated, the glucocorticoid regimen, and the name and telephone number of the clinician.c

When surgery is required, importance of informing the attending physician, dentist, or anesthesiologist of recent (within 12 months) glucocorticoid therapy.c

Advise patients receiving orally inhaled glucocorticoid therapy who are currently being withdrawn or who have been withdrawn from systemic therapy to immediately resume full therapeutic dosages of systemic glucocorticoids and to contact their clinician for further instructions during stressful periods (e.g., severe infection, severe asthmatic attack).

In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs.

Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.ac

Importance of women informing clinicians if they are or plan to become pregnant or to breast-feed.a

Importance of informing patients of other important precautionary information.ac (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

o. Centers for Disease Control and Prevention. General recommendations on immunization: recommendations of the Advisory Committee on Immunization Practices and the American Academy of Family Physicians. MMWR. 2002; 51(RR-2):1-44